Schematic representation of suggested child-adult differences in muscle contractility stemming from differential motor-unit activationparisons of size-normalized muscular force, velocity (solid lines), and power (dashed lines) relationships are shown
Table 1 summarizes the evidence presented in this review, indicating the likelihood of acknowledged muscle functional factors of accounting for the various known child-adult functional and metabolic differences. While some factors, notably muscle composition, can account for a considerable portion of the observed differences, only the differential motor-unit activation hypothesis can account for all of them. As illustrated in Figure 2 , children’s size-normalized maximal force, velocity, and power are all lower than the respective adult values. Moreover, the age-related difference in maximal velocity is greater than the respective difference in maximal force. As power is a product of force and velocity, children’s maximal power is further compromised, compared with adults, than either force or velocity.
Figure 2 provides a schematic graphic illustration of the proposed child-adult muscle-contractile differences, as would be manifested in force-velocity and force- power relationships
Numerous factors may be involved in many of the reviewed child-adult differences. As shown in Table 1 , these differences can largely or fully be explained by three main factors: muscle fiber composition, metabolic profile, and motor-unit activation. In some cases (e.g., children’s lower muscular power or greater endurance), the relative contribution of these factors cannot be untangled and the observed differences can be explained by any one, two, or all three factors. In other cases, it may be possible to dismiss metabolic profile differences, but neither of the other two factors (e.g., children’s lower instantaneous force or RFD). Differential muscle composition is impossible to dismiss in explaining all but one observation, namely, the differential response to resistance training. The nature of this response can only be explained by children’s lower level of volitional muscle activation.
The lower overall muscle activation, as suggested by volitional vs. nonvolitional force production, cannot be directly distinguished from specific lower activation of type-II motor units. This is mainly where direct, conclusive evidence is still lacking. However, the size principle of motor-unit recruitment suggests that overall lower activation is more reflective of lower type-II motor unit activation. The disproportionately-low lactate response to maximal short-term exercise is another strong if indirect evidence that higher-threshold, type-II motor units are less activated in children.
It is likely premature to speculate on the exact mechanism responsible for children’s postulated lower capacity to employ type-II motor units. A conceptual approach might involve the neuromotor impulse generation in the motor cortex. Possibly, there is a low ceiling of motoneuron impulse frequency during early development, which gradually rises with maturation. A low impulse frequency would mamba preselect type-I motor-unit activation to the exclusion or curtailment of type-II motor-units. Contrary to what is known in adults, children’s type-II muscle-fibers were shown to be similar or even smaller in diameter / cross-sectional area than type-I fibers (21,92). This strongly suggests extensive under-use of type-II motor-units during prepubescence. Moreover, these findings may be related to those of lower type-II muscle-fiber composition during early childhood (54,63). That is, a low ceiling of neuromotor impulse frequency may in effect produce type-I phenotypes of fibers that are destined to become type-II. Indeed, early studies involving modification of neural activation in young animals indicated that it is the nature of neural activation which determines the phenotypic and contractile properties of the motor unit (22). A gradual increase in motoneuron impulse frequency during maturation could thus be the factor responsible not only for increasing utilization of type-II motor units, but for the transformation of type-I to type-II fibers during growth (54,63) as well. This then would explain findings of higher type-I muscle-fiber composition in children (54,63), and their associated effects on the muscle’s metabolic profile.